Hamilton D H, Moyer R W, Moyer S A
J Gen Virol. 1980 Aug;49(2):273-87. doi: 10.1099/0022-1317-49-2-273.
Rabbit cornea cells (RC-60) restrict the reproduction of vesicular stomatitis virus (VSV) (Thacore & Youngner, 1975). In cells infected with VSV alone, an inhibition in the synthesis of VSV genome RNA is observed. A number of parameters which could affect virus RNA synthesis have been examined: virus transcription and post-transcriptional modification, translation, modification of proteins and migration of the G protein to the surface of the cell; they all appear to be normal, although somewhat diminished, in the restricted system. In these cells, therefore, it is the replication of VSV RNA that is directly inhibited, although limited synthesis of both (+) and (-) strand genome length RNA does occur. When the cells are co-infected with rabbit poxvirus (RPV) as a helper virus, however, VSV production is normal. Our studies suggest that RPV plays a role in the maturation as well as in the replication of VSV RNA in RC-60 cells. Certain mutants of RPV have been found to lack the helper function and are unable to convert the RC-60 cells into a permissive host for VSV. These mutants should facilitate the elucidation of the mechanism by which RPV is able to overcome the restriction in these cells.
兔角膜细胞（RC - 60）可限制水疱性口炎病毒（VSV）的繁殖（萨科尔和扬纳，1975年）。在仅感染VSV的细胞中，可观察到VSV基因组RNA合成受到抑制。已对一些可能影响病毒RNA合成的参数进行了检测：病毒转录和转录后修饰、翻译、蛋白质修饰以及G蛋白向细胞表面的迁移；在受限系统中，尽管这些过程均有所减弱，但似乎均正常。因此，在这些细胞中，直接受到抑制的是VSV RNA的复制，不过确实会发生有限的（+）链和（-）链基因组长度RNA的合成。然而，当这些细胞与兔痘病毒（RPV）作为辅助病毒共同感染时，VSV的产生是正常的。我们的研究表明，RPV在RC - 60细胞中VSV RNA的成熟以及复制过程中均发挥作用。已发现某些RPV突变体缺乏辅助功能，无法将RC - 60细胞转变为VSV的允许性宿主。这些突变体应有助于阐明RPV能够克服这些细胞中限制的机制。
